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F.S.R. Roitberg
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P3.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 235)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/09/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P3.04-109 - Validating ECOG Performance Status as a Prognostic Factor in Brazilian Patients with Pulmonary Adenocarcinoma (ID 1589)
09:30 - 09:30 | Author(s): F.S.R. Roitberg
- Abstract
Background:
ECOG performance status scale (ECOG) is a score used in clinical practice to estimate cancer patients´ functionality, and its value as a prognostic factor has been extensively demonstrated. Patients (pts) harboring EGFR mutations have been experiencing substantial improvements in their functionality and ECOG after receiving targeted therapies with tyrosine kinase inhibitors (TKIs). Recently, with the availability of TKIs for the treatment of pts harboring EGFR mutations, a treatment capable of inducing marked improvements in patients´ functionality, it is pertinent to access the prognostic value of ECOG (at the moment of the diagnosis of cancer) for these pts. In this scenario, we aimed to validate ECOG as a prognostic factor in a population of Brazilian pts with pulmonary adenocarcinoma, including those harboring EGFR mutations who received treatment with TKIs.
Methods:
This is a retrospective, uniinstitutional study of all consecutively tested tissue samples from 417 pts diagnosed with pulmonary adenocarcinoma treated at our Institution. All samples were formalin-fixed and paraffin-embedded. Tumor areas were selected and macrodissected, followed by whole DNA extraction and amplification by PCR. EGFR genotyping was performed through DNA sequencing (exons 18, 19, 20 and 21) by Sanger´s methodology. Pts were treated according to their clinician´s choice: TKIs (Erlotinib or Gefitinib) were available for pts harboring EGFR mutations, and those harboring wild type EGFR were treated with chemotherapy.
Results:
417 pts had tumor samples genotyped between Aug/2011 and Sep/2015. Median age was 62 y (17-91), and 237 (57%) were female. According to ethnicity, 357 pts were Caucasian (86%), 37 African-American (9%) and 21 Asian (5%); 140 pts were classified as never-smokers (34%), 37 (9%) as light-smokers (≤ 10 packs/year.) and 238 (57%) as current smokers (> 10 packs/year). EGFR activating mutations were identified in 103 out of 417 samples (24.7%). Among patients harboring EGFR mutations, median survival, in months (m), according to ECOG performance status was: 25.1m for ECOG 0, 19.5m for ECOG 1, 10.5m for ECOG 2, 5.9m for ECOG 3, and <1m for ECOG 4. Among patients with wild-type EGFR, median survival, in months, according to ECOG was: 112.8m for ECOG 0, 20.1m for ECOG 1, 8.8m for ECOG 2, 5.7m for ECOG 3, and 2m for ECOG 4. Among those pts with stage IV adenocarcinoma and ECOG-PS 0-1, with a median follow-up of 12 months, the median overall survival rate was 16.3 months for pts harboring EGFR-activating mutations, and 14.5 months for those with EGFR-wild-type tumors (HR 0.99, p=0.93, 95%CI 0.73-1.33). On multivariate analysis, ECOG-PS > 1 increased 1.59 times the risk of death (HR 1.59, 95%CI 1.41-1.78) regardless of EGFR-mutational status.
Conclusion:
Our data has validated ECOG performance status as a prognostic factor in this Brazilian population of pulmonary adenocarcinoma pts, independent of EGFR mutational status. As a practical and reproducible scale, ECOG remains a valuable tool to guide clinical decisions and estimate cancer patients´ prognosis, even with the advent of Tyrosine kinase inhibitors.
